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Gingival biopsies from areas characterized as clinically normal, mild gingivitis, or periodontitis were examined. Immunoglobulin (IgG, IgA, IgM, IgE and IgD) bearing cells at the sulcular and oral epithelium -lamina propria junctions as well as the central lamina propria areas were quantitated. Normal gingiva (P. I. = 0-0.2) contained few lymphocytes and plasma cells. Biopsies from areas of mild gingivitis (P.I. = 0.2-1) were infiltrated at the sulcular epithelium -lamina propria junction by lymphocytes lacking membraneassociated immunoglohulins (94 %). Few plasma cells were evident. In contrast, tissue associated with periodontitis (P. I. = 4.0-8.0) contained significant numbers of immunoglobulin hearing lymphocytes (78 %, IgG; 9 %, IgM; and 4 % IgA) and plasma cells (67 %, IgG; 24 %, IgM; and 8 % IgA) distributed throughout all three major tissue areas.These findings indicated that the nature of cellular infiltrates differed in mild gingivitis and periodontitis. The presence of predominantly IgG and IgM containing cells in periodontitis had important implications for the contribution of nonspecific effector mechanisms to the destruction of periodontal tissue. infiltrate has not been resolved. Compara-

A human isolate of type A Hong Kong influenza virus (H3N2) was adapted to mice by serial passage. Lung homogenates from mice who received low passage levels contained about the same quantity of virus (10 6.2−6.95 50% tissue culture infective doses/ml) as those from mice who received high passage levels (10 5.95−6.45 50% tissue culture infective doses/ml); however, death occurred only in animals given high-passage virus. Passage 3 (P3) and passage 9 (P9) viruses were selected as representative of low-passage and high-passage viruses, respectively. Although minimal differences were detected in infectivity for rhesus monkey kidney tissue cultures and mice, P9 virus was at least 10,000 times more lethal for mice (mean lethal dose = 10 4.2 ). Infection with P3 virus was accompanied by minimal bronchitis and bronchiolitis only, whereas P9-infected animals exhibited marked bronchitis, bronchiolitis, and pneumonia. Striking thymic cortical atrophy was also demonstrable in the P9-infected animals and, although virus was more commonly recovered from thymuses from these animals, immunofluorescent studies revealed only a few cells containing influenza virus antigens. To further explore the participation of thymus-derived lymphocytes in influenza, athymic nude mice and furred immunocompetent littermates were given 500 50% mouse infectious doses of P9 virus. Nude mice exhibited an increased survival time and, in contrast to the extensive lung pathology seen in furred littermates, manifested minimal cellular infiltration and no tissue destruction in lungs. Brains from nude mice exhibited encephalomalacia with lymphocytic perivascular cuffing, which was not seen in furred animals. Virus was recovered from brains of 6 of 13 nude mice and 1 of 10 furred animals. The contrasting models suggest that thymus-dependent cells play a significant role in the inflammatory response to influenza virus infection and should prove useful for probing host-virus interactions which characterize influenza virus virulence.

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A B S T R A C T Iroin-deficien1t rats halve an1 im11paired work performancice, even when their aniemiiia is correcte(d by exchanige transfusioin. Muscle activity is associate(l with a higher blood lactate concenltrationi thani is observed in iron-replete aniimals. The accumulation of lactate is a result of excessive productioni as lactate clearancie fromn the 1)loo0( was shown to be unaffecte(l. By acljusting the work loa(l to a lower level, it was possible to (livide iron-deficient animilals into two groups, oine capal)le of continued treadlmiill runninig and aniother in which aniimals stoppe(d before 20( min. In the former, blood lactate conicenitrationi reache(d a plateau at moderate levels, whereas it coontiniued to increase in the latter until the anIimial stopped runninig. Levels ofa-glycerophosphate oxidase in skeletal mulscle mitochondria were found( to be mulch lower in the secon(d group (P < 0.001). Lactate infusioin into normiial animals was showin to interfere with work performiiance, anid muainteinance of a normiial pH in iron-deficieint anid iron-replete animiials didinot prevent the impairment in work associated with high bloo(1 lactate concentrations. Additional evidenlce Wcas obtained that energy substrate (blood glucose anid free fatty acids, muscle glycogen) was adequate in irondeficient animiials. Oxygein tension in their vena caval blood was higher than in controls. Fuirthermore, the in situ behavior of electrically stimulated gastrocnemius and soleus muscles appeared similar to that of control animals. Because the stimulation of the single muscle in the iron-deficient animal did not result in appreciable elevation of blood lactate andl did not show impaired contractility further supported the hypothesis that the elevation ofblood lactate caused the decreased work performance. It is concluded that iron deficiency by a depletion in the iron-containing mitochondrial enzyme, a-glycerophosphate oxidase,

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Iron-deficient rats become hypothermic and have an excessive catecholamine response when exposed to an ambient temperature of 4 degrees C. This is not due to changes in body insulation, since thickness is unaltered, since differences persist after removal of hair, and since cutaneous vasoconstriction is intact. On the other hand, oxygen consumption of iron-deficient animals at 4 degrees C is reduced, 39 +/- 3 ml . kg-1 . min-1 compared to 63 +/- 2 in control animals. Thyroxine (T4) values at 4 degrees C were 4.34 +/- 0.20 microgram/dl sera as compared to control values of 3.6 +/- 0.32. Triiodothyronine (T3) values of iron-deficient animals in the cold were 48 +/- 6.8 ng/dl as compared to 72 +/- 5.6 in control animals. Treatment of iron-deficient animals with iron was shown to normalize the plasma T3 response at 4 degrees C within 6 days. Thyroidectomized iron-deficient animals injected with T3 did not show hypothermia at 4 degrees C, whereas thyroidectomized iron-deficient animals injected with T4 showed hypothermia, increased catecholamines, and decreased T3 levels as compared to non-iron-deficient animals similarly treated. It is proposed that iron deficiency impairs conversion of T4 to T3 and that this is primarily responsible for the hypothermia observed.

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